PRECLINICAL
PHASE 1
PHASE 2
PHASE 3

RSLV-132

Sjögren’s Syndrome
Systemic Lupus Erythematosus
PASC       ME/CFS

RSLV-145

Systemic Lupus Erythematosus
Lupus Nephritis

RSLV-621

Systemic Lupus Erythematosus
Lupus Nephritis
Systemic Sclerosis

RSLV-132

RSLV-132, our lead product candidate, is a novel compound that eliminates inflammatory nucleic acids, which are known to accumulate in lupus and Sjögren’s syndrome patients and cause chronic inflammation.

RSLV-621

RSLV-621 is an Fc-fusion protein consisting of the IFNAR1 and IFNAR2 subunits of the type I interferon receptor.  It is a potent (sub-nanomolar) inhibitor of type I interferons.  The recent launch of anifrolumab has demonstrated the clinical importance of inhibiting type I interferons in SLE and has provided a regulatory roadmap for other interferon antagonists.  A phase 1 POC study in SLE patients is planned with RSLV-621 and will provide safety and tolerability data as well as the degree of interferon signature knockdown.  If the interferon signature is significantly inhibited in this study a large P2 will be embarked on.

RSLV-145

This compound is a prototype of a platform of nuclease Fc fusion proteins Resolve scientists have created that have both RNase catalytic activity and DNase catalytic activity. We have engineered the nucleases in multiple different formats that give rise to numerous therapeutic applications. These are potent antagonists of the inflammatory properties of both RNA and DNA with potential therapeutic utility in lupus, lupus nephritis, vasculitis and autoimmune diseases that involve NETosis. The death of neutrophils often creates a dense lattice of DNA and RNA which forms a scaffold for autoantigens that bind to autoantibodies present in the blood of patients with autoimmune disease. By digesting neutrophil NETS, RSLV-145 eliminates the scaffold holding these autoantigens together and prevents the concentrated activation of the immune system at that point. In the case of vasculitis, the NETS are present on the vascular endothelium and causes severe vascular inflammation characteristic of this disease. Similar pathogenic nucleic acids have been observed in lupus and lupus nephritis.